I'm not gonna argue that one,
yes i am
there are dozens (if not hundreds) of published articles about leaky gut, many relating it to autoimmune disease.
The scientific debate seems to be about whether it is a 'syndrome' or not
"Review article: Intestinal permeability in Crohn's disease.
Aliment Pharmacol Ther 1997 Dec;11 Suppl 3:47-53; discussion 53-6
Meddings JB
Gastrointestinal Research Group, University of Calgary, Alberta, Canada.
SUMMARY
Measurements of intestinal permeability (IP) may help in determining susceptibility for the development of Crohn's disease or for imminent relapse in patients with the disease. It is now apparent that a subset of patients at high risk for the development of Crohn's disease have either increased baseline IP or an exaggerated response to environmental agents that increase IP. These, coupled with observations that increased IP in patients at risk for the development of Crohn's disease is associated with an abnormal immunological phenotype, lend support to the hypothesis that
increased IP is a very early event in the genesis of Crohn's disease."
"
Increased Intestinal Permeability in Patients with Crohn's Disease and Their Relatives
A Possible Etiologic Factor
DANIEL HOLLANDER, M.D.;
CONSTANCE M. VADHEIM, Ph.D.;
EDWARD BRETTHOLZ, M.D.;
GLORIA M. PETERSEN, Ph.D.;
THOMAS DELAHUNTY, Ph.D.; and
JEROME I. ROTTER, M.D.
+ Author Affiliations
Irvine and Los Angeles, California
Abstract
The cause of Crohn's disease is unknown, although
alterations in intestinal permeability may play a primary role. Because we were interested in permeability changes that occur before the onset of intestinal inflammation, we took advantage of the known genetic predisposition to this disease and studied not only patients with Crohn's disease, but their clinically unaffected relatives as well. Intestinal permeability was assessed using the marker polyethylene glycol-400 ingested with a standard meal. We found that 17 normal volunteers absorbed 215 ± 29.6 mg (mean ± SE), whereas 11 patients with Crohn's disease absorbed 514 ±94.7 mg and their 32 healthy relatives absorbed 566 ±62.4 mg. The twofold increase in permeability of patients and their relatives (p <0.005 compared with controls) indicates that the intestinal defect in the ability to exclude larger sized molecules is
not secondary to clinically recognized intestinal inflammation, but
is a primary defect that may be an etiologic [that means causative]
factor in this disease."
Role of the intestinal barrier in inflammatory bowel disease
Mike G Laukoetter, Porfirio Nava, Asma Nusrat
Mike G Laukoetter, Porfirio Nava, Asma Nusrat, Epithelial Pathobiology Research Unit, Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA 30322, United States
Mike G Laukoetter, Department of General Surgery, University of Muenster, Muenster 48149, Germany
Supported by Grants from the German Research Foundation (Deutsche Forschungsgemeinschaft La 2359/1-1 to M.L.), National Institutes of Health (DK 55679, DK 59888 to A.N.) and Crohn’s and Colitis Foundation of America (to A.N.)
Correspondence to: Asma Nusrat, Department of Pathology and Laboratory Medicine, Emory University, Whitehead Research Building, Room 105E, 615 Michael Street, Atlanta, GA 30322, United States.
[email protected]
Abstract
A critical function of the intestinal mucosa is to form a barrier that separates luminal contents from the interstitium. The single layer of intestinal epithelial cells (IECs) serves as a dynamic interface between the host and its environment. Cell polarity and structural properties of the epithelium is complex and is important in the development of epithelial barrier function. Epithelial cells associate with each other via a series of intercellular junctions. The apical most intercellular junctional complex referred to as the Apical Junction Complex (AJC) is important in not only cell-cell recognition, but also in the regulation of paracellular movement of fluid and solutes. Defects in the intestinal epithelial barrier function have been observed in a number of intestinal disorders such as inflammatory bowel disease (IBD).
It is now becoming evident that an aberrant epithelial barrier function plays a central role in the pathophysiology of IBD. Thus, a better understanding of the intestinal epithelial barrier structure and function in healthy and disease states such as IBD will foster new ideas for the development of therapies for such chronic disorders.
© 2008 WJG. All rights reserved.
A role for Campylobacter jejuni-induced enteritis in inflammatory bowel disease?
Lisa D. Kalischuk1 and
Andre G. Buret2
+ Author Affiliations
1Agriculture and Agri-Food Canada, Lethbridge;
2Department of Biological Sciences, Inflammation Research Network, University of Calgary, Calgary, Alberta, Canada
Address for reprint requests and other correspondence: A. G. Buret, Dept. of Biological Sciences, Inflammation Research Network, Univ. of Calgary, 2500 Univ. Dr. N. W., Calgary, AB, Canada, T2N 1N4 (e-mail:
[email protected]).
Submitted 26 May 2009.
accepted in final form 25 October 2009.
Abstract
The inflammatory bowel diseases (IBD), Crohn's disease and ulcerative colitis, are T cell-mediated diseases that are characterized by chronic, relapsing inflammation of the intestinal tract. The pathogenesis of IBD involves the complex interaction between the intestinal microflora, host genetic and immune factors, and environmental stimuli. Epidemiological analyses have implicated acute bacterial enteritis as one of the factors that may incite or exacerbate IBD in susceptible individuals. In this review, we examine how interactions between the common enteric pathogen Campylobacter jejuni (C. jejuni), the host intestinal epithelium, and resident intestinal microflora may contribute to the pathogenesis of IBD. Recent experimental evidence indicates that C. jejuni may permit the translocation of normal, noninvasive microflora via novel processes that implicate epithelial lipid rafts.
This breach in intestinal barrier function may, in turn, prime the intestine for chronic inflammatory responses in susceptible individuals. Insights into the interactions between enteric pathogens, the host epithelia, and intestinal microflora will improve our understanding of disease processes that may initiate and/or exacerbate intestinal inflammation in patients with IBD and provide impetus for the development of new therapeutic approaches for the treatment of IBD.
from Sydney Morning Herald website
http://www.smh.com.au/articles/2004/07/08/1089000262822.html?from=moreStories
Professor Ian Brighthope, president of the Australian College of Nutritional and Environmental Medicine, says
leaky gut is well documented as an abnormal physiology. "
Leaky gut is a real phenomenon. It does occur, there's no doubt about that,"
Dr Peter Katelaris, clinical associate professor at the University of Sydney and gastroentorologist at Concord Hospital, agrees. "We recognise leaky gut as a consequence of a disease," he says, emphasising that his view is from an evidence-based medical perspective. "People have a leaky gut for a variety of medical, scientific reasons. When you talk about leaky gut syndrome you're defining a syndrome that is a bit nebulous.
"There's a lot of speculation that there is the potential for harmful things to come across [the lining of the gut] but usually it is another disease that is the problem."
Katelaris says increased gut permeability is prevalent in patients with Crohn's disease and coeliac disease.
to quote wikipedia
"Defects in the intestinal epithelial barrier function have been observed in a number of bowel disorders such as inflammatory bowel disease (IBD). It is now becoming evident that
an aberrant epithelial barrier function plays a central role in the pathophysiology of IBD, gastrointestinal diseases, cardiovascular disease, acute and chronic pediatric and other recognised diseases."
If those people with 15 years or more of remission aren't "cured" then i don't know who is.
You have to remember that crohn's an IBD are worth an estimated 2 billion dollars a year to big pharma,
Do you really think they want you to get well?
